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人参麦冬提取物(SMF)对缺血心肌组织中蛋白质S-亚硝基化的影响

[Effects of Radix Ginseng and Radix Ophiopogonis extract (SMF) on protein S-nitrosylation in ischemic myocardial tissue].

作者信息

Feng Jin-hong, Shi Qiang, Wang Yi, Cheng Yi-yu

机构信息

Zhejiang University, Department of Chinese Medicine Science & Engineering, Hangzhou 310058, China.

出版信息

Zhongguo Zhong Yao Za Zhi. 2008 Aug;33(15):1894-7.

Abstract

OBJECTIVE

To observe the effect of Radix Ginseng and Radix Ophiopogonis extract (SMF) on protein S-nitrosylation in rats myocardial with ischemia/reperfusion injury (MI/RI).

METHOD

Myocardial ischemia/reperfusion in rats were produced by occlusion of the left anterior descending coronary artery. To study the cardioprotective effects of SMF on the acute MI/RI rats, the serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), and nitric oxide (NO) were determined. The change of the expression of endothelial nitric oxide synthase (eNOS) was detected by Western blot. The content of related S-nitrosylation proteins in myocardial tissue was measured by Biotin-Switch method.

RESULT

SMF significantly decreased the serum levels of CK and LDH as well as increased the serum levels of NO and the expression of eNOS in myocardial tissue. The contents of S-nitrosylation proteins were significantly increased from (4.42 +/- 0.60) micromol x g(-1) to (8.78 +/- 1.37) micromol x g(-1). The molecular weight of the majority S-nitrosylation proteins were in the range of 90 x 10(3)-117 x 10(3).

CONCLUSION

Increased expression of eNOS and NO induced by SMF may activate S-nitrosylation of many proteins in rat hearts. The change of the activities or functions of those proteins by S-nitrosylation may be an important mechanism for myocardial protective effects of SMF.

摘要

目的

观察人参麦冬提取物(SMF)对缺血/再灌注损伤(MI/RI)大鼠心肌蛋白S-亚硝基化的影响。

方法

通过结扎左冠状动脉前降支制备大鼠心肌缺血/再灌注模型。为研究SMF对急性MI/RI大鼠的心脏保护作用,测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)和一氧化氮(NO)水平。采用蛋白质免疫印迹法检测内皮型一氧化氮合酶(eNOS)表达的变化。采用生物素转换法测定心肌组织中相关S-亚硝基化蛋白的含量。

结果

SMF显著降低血清CK和LDH水平,同时提高血清NO水平及心肌组织中eNOS的表达。S-亚硝基化蛋白含量从(4.42±0.60)μmol·g⁻¹显著增加至(8.78±1.37)μmol·g⁻¹。大多数S-亚硝基化蛋白的分子量在90×10³-117×10³范围内。

结论

SMF诱导的eNOS和NO表达增加可能激活大鼠心脏中多种蛋白的S-亚硝基化。这些蛋白通过S-亚硝基化导致的活性或功能变化可能是SMF发挥心肌保护作用的重要机制。

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